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- W2183338547 abstract "We recently reported that canine pulmonary microsomes metabolize arachidonic acid to all four regioisomeric epoxyeicosatrienoic acids (EET). 5,6-EET dilates blood vessels in several nonpulmonary vascular beds, often in a cyclooxygenase-dependent manner. The present study was designed to determine whether 5,6-EET can decrease pulmonary vascular resistance (PVR) in the intact pulmonary circulation. In isolated canine lungs perfused with physiological salt solution, a constant infusion of U-46619 (3.28 ± 0.99 nmol/min) increased PVR 62.1 ± 4.5%. Administration of 5,6-EET (10 −5 M) into the perfusate reduced the U-46619-mediated increase in PVR by 23.6 ± 6.1%. These effects of U-46619 and 5,6-EET were limited to changes in resistance solely in the pulmonary venous segment. In contrast, venous as well as arterial segmental resistances were increased in 5-hydroxytryptamine (5-HT)-treated lungs. However, in the latter instance, 5,6-EET reduced arterial but not venous segmental resistance. 5,6-EET increased pulmonary PGI 2 synthesis from 70.5 ± 18.4 to 675.9 ± 125.4 ng/min. In the presence of indomethacin (10 −4 M), 5,6-EET did not increase PGI 2 synthesis nor did it decrease U-46619- or 5-HT-mediated increases in PVR. In canine intrapulmonary vessels, 5,6-EET decreased active tension in veins contracted with U-46619. 5,6-EET decreased active tension in arteries but not veins contracted with 5-HT, consistent with results in the perfused lungs. These results demonstrate that 5,6-EET is a vasodilator in the intact pulmonary circulation. Its dilator activity depends on the constrictor agent present, the segmental resistance, and cyclooxygenase activity." @default.
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- W2183338547 date "1998-07-01" @default.
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- W2183338547 title "5,6-Epoxyeicosatrienoic acid reduces increases in pulmonary vascular resistance in the dog" @default.
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- W2183338547 doi "https://doi.org/10.1152/ajpheart.1998.275.1.h100" @default.
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